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Advanced Research in Cardiopulmonary Injury
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Advanced Research in Cardiopulmonary Injury

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 5060

Special Issue Editor

Dr. Rui Song

E-Mail Website
Guest Editor
Loma Linda University School of Medicine, Loma Linda, CA, USA
Interests: cardiopulmonary development; regeneration; remodeling; epigenetics; genetics; mitochondria

Special Issue Information

Dear Colleagues,

Cardiopulmonary disease refers to a range of severe conditions affecting the heart ("cardio") and lungs ("pulmonary"). Epidemiological studies have revealed that many environmental and maternal factors (such as high altitude, smoking, chorioamnionitis, and hypertension/preeclampsia) and fetal factors (such as placental abruption, cord prolapse, and low birth weight) interact during fetal development. As a result of these risk factors, maternal–fetal morbidity and developmental plasticity are altered, and cardiopulmonary injury and repair processes in the fetus and newborn infant lead to adult-onset systemic pulmonary or cardiovascular conditions. During the development and morphogenesis of cardiopulmonary tissues, the molecular mechanisms involved rely on genetics and epigenetics and signaling crosstalk in regulating cell survival, growth, proliferative activity, and differentiation. Pathological phenotypes can result from the abnormal regulation of any of these processes.

This Special Issue of the International Journal of Molecular Sciences focuses on the field of cardiopulmonary injury, and welcomes both original research articles and review papers that deal with the molecular mechanisms linking to developmental cardiopulmonary disease, as well as potential therapeutic interventions for cardiopulmonary growth/developmental disorder.

Dr. Rui Song
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiopulmonary development
  • chronic diseases
  • regeneration
  • remodeling
  • epigenetics
  • genetics
  • mitochondria

Published Papers (3 papers)

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Research

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11 pages, 2150 KiB  
Article
Identification of SALL4 Expressing Islet-1+ Cardiovascular Progenitor Cell Clones
by Andrea Monteon, Lorelei Hughes, Victor Camberos and Mary Kearns-Jonker
Int. J. Mol. Sci. 2023, 24(2), 1780; https://doi.org/10.3390/ijms24021780 - 16 Jan 2023
Cited by 1 | Viewed by 1208
Abstract
The utilization of cardiac progenitor cells (CPCs) has been shown to induce favorable regenerative effects. While there are various populations of endogenous CPCs in the heart, there is no consensus regarding which population is ideal for cell-based regenerative therapy. Early-stage progenitor cells can [...] Read more.
The utilization of cardiac progenitor cells (CPCs) has been shown to induce favorable regenerative effects. While there are various populations of endogenous CPCs in the heart, there is no consensus regarding which population is ideal for cell-based regenerative therapy. Early-stage progenitor cells can be differentiated into all cardiovascular lineages, including cardiomyocytes and endothelial cells. Identifying an Islet-1+ (Isl-1+) early-stage progenitor population with enhanced stemness, multipotency and differentiation potential would be beneficial for the development of novel regenerative therapies. Here, we investigated the transcriptome of human neonatal Isl-1+ CPCs. Isl-1+ human neonatal CPCs exhibit enhanced stemness properties and were found to express Spalt-like transcription factor 4 (SALL4). SALL4 plays a role in embryonic development as well as proliferation and expansion of hematopoietic progenitor cells. SALL4, SOX2, EpCAM and TBX5 are co-expressed in the majority of Isl-1+ clones isolated from neonatal patients. The pre-mesendodermal transcript TFAP2C was identified in select Isl-1, SALL4, SOX2, EpCAM and TBX5 expressing clones. The ability to isolate and expand pre-mesendodermal stage cells from human patients is a novel finding that holds potential value for applications in regenerative medicine. Full article
(This article belongs to the Special Issue Advanced Research in Cardiopulmonary Injury)
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20 pages, 2959 KiB  
Article
Restoration of Mitochondrial Function Is Essential in the Endothelium-Dependent Vasodilation Induced by Acacetin in Hypertensive Rats
by Yuan Li, Qingya Dang, Zhiyi Li, Chuting Han, Yan Yang, Miaoling Li and Pengyun Li
Int. J. Mol. Sci. 2022, 23(19), 11350; https://doi.org/10.3390/ijms231911350 - 26 Sep 2022
Cited by 3 | Viewed by 1681
Abstract
Mitochondrial dysfunction in the endothelium contributes to the progression of hypertension and plays an obligatory role in modulating vascular tone. Acacetin is a natural flavonoid compound that has been shown to possess multiple beneficial effects, including vasodilatation. However, whether acacetin could improve endothelial [...] Read more.
Mitochondrial dysfunction in the endothelium contributes to the progression of hypertension and plays an obligatory role in modulating vascular tone. Acacetin is a natural flavonoid compound that has been shown to possess multiple beneficial effects, including vasodilatation. However, whether acacetin could improve endothelial function in hypertension by protecting against mitochondria-dependent apoptosis remains to be determined. The mean arterial pressure (MAP) in Wistar Kyoto (WKY) rats, spontaneously hypertensive rats (SHR) administered with acacetin intraperitoneally for 2 h or intragastrically for six weeks were examined. The endothelial injury was evaluated by immunofluorescent staining and a transmission electron microscope (TEM). Vascular tension measurement was performed to assess the protective effect of acacetin on mesenteric arteries. Endothelial injury in the pathogenesis of SHR was modeled in HUVECs treated with Angiotensin II (Ang II). Mitochondria-dependent apoptosis, the opening of Mitochondrial Permeability Transition Pore (mPTP) and mitochondrial dynamics proteins were determined by fluorescence activated cell sorting (FACS), immunofluorescence staining and western blot. Acacetin administered intraperitoneally greatly reduced MAP in SHR by mediating a more pronounced endothelium-dependent dilatation in mesenteric arteries, and the vascular dilatation was reduced remarkably by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis. While acacetin administered intragastrically for six weeks had no apparent effect on MAP, it improved the endothelium-dependent dilatation in SHR by activating the AKT/eNOS pathway and protecting against the abnormalities of endothelium and mitochondria. Furthermore, acacetin remarkably inhibited Ang II induced apoptosis by inhibiting the increased expression of Cyclophilin D (CypD), promoted the opening of mPTP, ROS generation, ATP loss and disturbance of dynamin-related protein 1 (DRP1)/optic atrophy1 (OPA1) dynamics in HUVECs. This study suggests that acacetin protected against endothelial dysfunction in hypertension by activating the AKT/eNOS pathway and modulating mitochondrial function by targeting mPTP and DRP1/OPA1-dependent dynamics. Full article
(This article belongs to the Special Issue Advanced Research in Cardiopulmonary Injury)
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Review

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15 pages, 685 KiB  
Review
Current Therapeutics for COVID-19, What We Know about the Molecular Mechanism and Efficacy of Treatments for This Novel Virus
by Divya Narayanan and Tanyalak Parimon
Int. J. Mol. Sci. 2022, 23(14), 7702; https://doi.org/10.3390/ijms23147702 - 12 Jul 2022
Cited by 3 | Viewed by 1829
Abstract
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) has caused significant morbidity and mortality worldwide. Though previous coronaviruses have caused substantial epidemics in recent years, effective therapies remained limited at the start of the Coronavirus disease 19 (COVID-19) pandemic. The emergence and rapid spread throughout [...] Read more.
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) has caused significant morbidity and mortality worldwide. Though previous coronaviruses have caused substantial epidemics in recent years, effective therapies remained limited at the start of the Coronavirus disease 19 (COVID-19) pandemic. The emergence and rapid spread throughout the globe of the novel SARS-CoV-2 virus necessitated a rapid development of therapeutics. Given the multitude of therapies that have emerged over the last two years and the evolution of data surrounding the efficacy of these therapies, we aim to provide an update on the major clinical trials that influenced clinical utilization of various COVID-19 therapeutics. This review focuses on currently used therapies in the United States and discusses the molecular mechanisms by which these therapies target the SARS-CoV-2 virus or the COVID-19 disease process. PubMed and EMBASE were used to find trials assessing the efficacy of various COVID-19 therapies. The keywords SARS-CoV-2, COVID-19, and the names of the various therapies included in this review were searched in different combinations to find large-scale randomized controlled trials performed since the onset of the COVID-19 pandemic. Multiple therapeutic options are currently approved for the treatment of SARS-CoV-2 and prevention of severe disease in high-risk individuals in both in the inpatient and outpatient settings. In severe disease, a combination of antiviral and immunomodulatory treatments is currently recommended for treatment. Additionally, anti-viral agents have shown promise in preventing severe disease and hospitalization for those in the outpatient setting. More recently, current therapeutic approaches are directed toward early treatment with monoclonal antibodies directed against the SARS-CoV-2 virus. Despite this, no treatment to date serves as a definitive cure and vaccines against the SARS-CoV-2 virus remain our best defense to prevent further morbidity and mortality. Full article
(This article belongs to the Special Issue Advanced Research in Cardiopulmonary Injury)
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